Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Step 1 AB > Immunology > Flashcards

Immunology Flashcards

1
Q

a. What muscles come from first arch?

b. what nerves come from first arch?

A

a. muscles of mastication, mylohyoid muscle, tensor tympani, tensor veli palatini
b. maxillary and mandibular division of trigeminal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What amino acids are found in elastin?

A

Glycine and proline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is mechanism of adenosine as anti-arrhythmic?

A

Increases outward K current
Hyper polarization of cells
Decreases intracellular Ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What part of the body drains to:

a. Axillary lymph node
b. Superificial inguinal nodes
c. Popliteal nodes

A

a. Upper limb, breast, skin above umbilicus
b. anal canal (below pectinate line), skin below umbilicus, scrotum
c. Dorsolateral foot, posterior calf

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which part of the GI tract drains to:

a. Celiac lymph nodes
b. Superior mesenteric nodes
c. Inferior mesenteric nodes
d. Internal iliac nodes

A

a. liver, stomach, spleen, pancreas, upper duodenum
b. lower duodenum, jejunum, ileum, colon to splenic flexure
c. colon from splenic flexure to upper rectum
d. lower rectum to anal canal (above pectinate line), bladder, vagina, prostate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which lymph nodes do the testes drain to? the scrotum?

A

Testes –> PARA-AORTIC

Scrotum –> superficial inguinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What part of the body does the right lymphatic duct drain?

A

Right side of body above the diaphragm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What part of the body does the thoracic duct drain?

A

Everything else besides right side of body above diaphragm. Goes into junction of left subclavian and internal jugular veins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do you find peer’s patches?

A

In lamina propria submucosa of ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

a. What muscles are derived from second branchial arch?

b. nerves from second branchial arch?

A

a. Muscles of facial expression, stapedius, stylohyoid

b. Cranial nerve seven

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which cells express MHCI?

A

ALL cells EXCEPT RBCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

a. What genes code for MHC I?

b. What genes code for MHC II?

A

a. HLA-A, B and C

b. HLA-DR, DP, and DQ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What diseases does HLA-B27 predispose to?

A 
PAIR
Psoriatic arthritis
Ankylosing spondylitis
Inflammatory Bowel Disease
Reactive arthritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What diseases do HLADR3/4 predispose to?

A

Diabetes mellitus type I

DR4 - Rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

a. What is Langerhans Cell Histiocytosis?
b. What markers does it express?
c. ON electron microscopy?
d. How does it present?

A

a. Group of proliferative disorders of dendritic cells
b. Express S-100 and CD1a
c. Birbeck granules
d. Presents as child with lytic bone lesion and skin rash or recurrent otitis media with mass involving mastoid bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What 4 things are expressed on dendritic cells?

A

B7
CD40
MHC I
MHC II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What mediates the following reactions:

a. hyperacute transplant rejection
b. acute transplant rejection
c. chronic rejection
d. graft vs. host

A

a. pre-existing recipient antibodies
b. T cells
c. T cells and Antibodies; Cytotoxic T cells treat transplant cells as self cells presenting non-self antigen - irreversible
d. Usually in BM transplants; the grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign proteins”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does graft vs. host disease present?

A

Maculopapular rash, jaundice

Diarrhea, hepatosplenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cyclosporine

a. Mechanism
b. Uses
c. Adverse effects (unique one?)

A

a. Binds to cyclophilin –> inhibits Calcineurin –> prevents production of IL2 –> disrupts T cell activation
b. Prevent transplant rejection, psoriasis, RA
c. Viral infections, lymphomas, NEPHROTOXICITY, HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tacrolimus

a. Mechanism
b. Uses
c. Adverse effects

A

a. Bind FK506 binding protein (FKBP) –> inhibits Calcineurin –> prevents production of IL2 –> blocks T cell activation
b. Transplant rejection prophylaxis
c. Increased risk of diabetes and neurotoxicity,, nephrotoxicity, HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Sirolimus

a. Mechanism
b. Uses
c. Adverse effects

A

a. binds FKBP –> inhibits mTOR –> inhibition of T cell proliferation and prevents response to IL2
b. Kidney transplant
c. Not that important - NOT NEPHROTOXIC; anemia, thrombocytopenia, leukopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Azathioprine

a. Mechanism
b. Use
c. Adverse effects

A

(precursor to 6-Mercaptopurine)

a. Inhibits lymphocyte proliferation by blocking nucleotide synthesis
b. Transplant rejection prophylaxis (especially kidney), RA, glomerulonephritis
c. BONE MARROW suppression; degraded by Xanthine Oxidase (toxic effects can be increased by Allopurinol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mycophenolate

a. Mechanism
b. Use

A

a. Inhibits IMP dehydrogenase –> prevents synthesis of guanine –> no cell replication/proliferation of B cells and T cells
b. Transplant patients and Lupus nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Muromonab

a. Mechanism
b. Use

A

a. Binds CD3 (T cells) –> interferes with T cell signal transduction –> shuts down T cells
b. Transplants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Daclizumab

a. Mechanism
b. Use

A

a. Binds to CD25 (IL2 receptor on activated T cells) –> blocks IL-2 signaling (Sirolimus is similar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Thalidomide

a. mechanism
b. use
c. toxicity

A

a. affects TNFa
b. Immunosuppression, anti-angiogenic
c. NOT USED - phocomelia, teratogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

a. What are the anti-TNFa agents?
b. What are they used for?
c. Which anti-TNF alpha drug is not a monoclonal antibody?

A

a. Adalimumab, Infliximab
b. Ankylosing spondylitis, RA, IBD, reactive arthritis
c. Etanercept - mimics TNFa receptor (gobbles up TNFa in circulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Abciximab

a. Mechanism
b. Use

A

a. Targets platelet glycoproteins IIb/IIIa
b. Anti-platelet agent for prevention of ischemic complications in patients undergoing percutaneous coronary intervention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Trastuzumab (Herceptin)

a. Mechanism
b. Use

A

a. Ab against HER2

b. Breast cancer that expresses HER2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Rituximab

a. Mech
b. Use

A

a. Targets CD20

b. B cell NON-Hodgkin lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Omalizumab

a. Mech
b. Use

A

a. Targets IgE

b. Severe asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Bruton agammaglobulinemia

a. defect
b. presentation
c. findings

A

a. defect in BTK (tyrosine kinase gene) –> no B cell maturation; X linked recessive
b. Recurrent bacterial infections and enteroviral infections after 6 months (decreased maternal IgG)
c. Absent B cells in peripheral blood, decrease IgG of ALL classes; absent lymph nodes/tonsils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Selective Ig Deficiency

a. Defect
b. Presentation
c. Findings

A

a. Most common primary immunodeficiency; unknown
b. Majority asymptomatic, can see airway and GI infections; autoimmune disease (atopy, asthma) anaphylaxis to IgA products
c. Decreased IgA with normal IgG and IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Common Variable Immunodeficiency

a. Defect
b. Presentation
c. Findings

A

a. Defect in B cell differentiation
b. Can be acquired in 20-30s, increased risk of autoimmune disease, bronchiectasis, lymphoma, sinopulmonary infections
c. decreased plasma cells, decreased immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Thymic aplasia (DiGeorge)

a. defect
b. presentation
c. findings

A

a. 22q11 deletion; failure to develop 3rd and 4th pharyngeal pouches –> absent parathyroids and thymus
b. Cardiac abnormality, Abnormal facies, Thymic aplasia, Cleft palate, Hypocalcemia - recurrent viral, fungal and protozoal infections
c. Decreased T cells, PTH and Calcium; absent thyme shadow on CXR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

IL-12 receptor deficiency

a. defect
b. presentation
c. findings

A

a. decreased TH1 response; AR
b. disseminated MYCOBACTERIAL and fungal infections;
c. Decreased IFNy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Chronic Mucocutaneous Candidiases

a. defect
b. presentation
c. findings

A

a. T cell dysfunction; many causes
b. non-invasive Candida albicans infections of skin and mucous membranes
c. absent cutaneous reaction and T cell proliferation in response to Candida antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Hyper IgM Syndrome

a. defect
b. presentation
c. findings

A

a. defective CD40L on Th cells –> defect in class switching; X linked recessive (3 types)
b. Severe pyogenic infections early in life; opportunistic infection with Penumocystis, Crypto, CMV
c. Increased IgM, decreased other antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SCID

a. defect
b. presentation
c. findings

A

a. defect in early stem cell differentiation; caused by many including adenosine deaminase deficiency (X linked)
b. failure to thrive, chronic diarrhea, thrush, recurrent viral/bacterial/fungal/protozoal infections (treat with BM transplant)
c. Decreased T cell receptor excision circles (TRECs); absence of thymic shadow, germinal centers, and T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Wiskott-Aldrich Syndrome

a. defect
b. presentatin
c. findings

A

a. Mutation in WAS gene (X linked) –> T cells unable to recognize actin cytoskeleton
b. Thrombocytopenia purpura, Eczema (on trunk), Recurrent infections
c. Decreased to normal IgG, IgM; Increased IgE and IgA; fewer/smaller platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the X linked immunodeficiencies?

A

Wiskott Aldrich
Bruton Agammaglobulinemia
Chronic granulomatous disease
Hyper-IgM syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Ataxia Telangiectasia

a. defect
b. presentation
c. findings

A

a. defects in ATM gene –> failure to repair DNA double strand breaks –> cell cycle arrest
b. Triad = Cerebellar defects (ATAXIA), spider Angiomas (telangiectasia) IgA deficiency
c. Increased AFP, decreased IgA, IgG an IgE; lymphopenia, cerebellar atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Chronic Granulomatous Disease

a. defect
b. presentation
c. findings

A

a. defect in NADPH oxidase –> decreased reactive oxygen species and respiratory burst in neutrophils
b. Increased susceptibility to catalase + organisms (Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia
c. Abnormal dihydroorhodamine test; nitroblue tetrazolium dye reduction test is negative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How is CGD treated?

A

Prophylactic TMP-SMX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Chediak-Higashi Disease

a. defect
b. presentation
c. findings

A

a. defective LYST gene –> defective lysosomal transport –> microtubule dysfunction in pharosome-lysosome fusion (AR)
b. Recurrent pyogenic infections by Staph and Strep; partial albinism, peripheral neuropathy, progressive neurodegeneration, infiltrative lymphohistiocytosis
c. giant granules in granulocytes and platelets, pancytopenia, coagulation defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Leukocyte adhesion deficiency type 1

a. defect
b. presentation
c. findings

A

a. defect in LFA-1 integrin (CD18) on phagocytes, impaired migration and chemotaxis (AR)
b. recurrent bacterial skin and mucosal infections, absent pus formation, impaired wound healing, delayed separation of umbilical cord
c. Increased neutrophils, absence of neutrophils at infection sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What cytokines do T helper cells produce to stimulate B cells?

A

IL4, IL5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the surface markers of B cells?

A

CD19, CD20, CD21, IgM, IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What cell markers do T cells have?

A

CD3, CD28, T cell receptor
Cytotoxic T cells have CD8
Helper T cells have CD4 and CD40L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What cell markers do NK cells have?

A

CD56 and CD16

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What cell markers do macrophages have?

A

CD14, MHC II, B7 protein, CD40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Which organism’s exotoxin works via each of the following mechanisms?

a. inactivates EF2
b. activates Gs
c. Disables Gi
d. Bacterial adenylat cyclase (No G protein involved)
e. Blocks GABA and glycine

A

a. Corynebacterium diptheriae, Pseudomonas (exotoxin A)
b. Vibrio cholerae, E. coli (ETEC heat labile toxin)
c. Pertussis toxin
d. Bacillus anthracis
e. Clostridium tetani (lockjaw)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What drug helps to make diagnosis of Myasthenia gravis?

A

Edrophonium (acetylcholinesterase inhibitor)

Too short acting to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What heart sound is associated with dilated CHF?

A

S3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What heart sound is associated with stiffened LV?

A

S4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is amyloidosis?

A

Accumulation of one specific protein in the tissues that aggregates into B pleated sheets which causes damage and apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is AL amyloidosis? What protein is deposited? Which organs does it affect?

A

(Primary)
Due to deposition of proteins from Ig Light chains
Can occurs as plasma cell disorder or associated with multiple myeloma.
Often affects multiple organ systems including renal (nephrotic syndrome), cardiac (restrictive CM, arrhythmia), hematologic (brushing, splenomegaly), GI (hepatomegaly) and neurologic (neuropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is AA amyloidosis? What protein is deposited? What is it associated with?

A

(Secondary)
Seen in chronic inflammatory conditions such as RA, IBD, spondyloarthropathy
Fibrils composed of serum Amyloid A; often multi system

59
Q

a. Patient with fibrils made of B2 microglobulin, ESRD and/or long term dialysis.
b. What else may it present as?

A

a. Dialysis-related amyloidosis

b. Carpal tunnel syndrome

60
Q

Which protein and fibril with each form of amyloidosis?

a. type 2 diabetes
b. Medullary thyroid CA
c. Alzheimer
d. Dialysis -associated

A

a. amylin, AIAPP
b. Calcitonin, A-CAL
c. B-amyloid, APP
d. B2 microglobulin, AB2M

61
Q

How do you diagnosis amyloidosis on biopsy?

A

Congo red stain; apple green birefringence

62
Q

Disease associated with anti-IgG antibodies

A

Rheumatoid arthritis

63
Q

Disease associated with anti-citrullinated protein antibodies (ACPA)

A

RA

64
Q

Associated with anti-centromere ABs

A

CREST Scleroderma

C for centromere, C for CREST

65
Q

Associated with Anti-Scl-70 Abs

A 
Diffuse Scleroderma
(Scl = Scleroderma)
66
Q

Associated with Anti-histone Abs

A

Drug-induced Lupus

67
Q

Associated with anti-nuclear Abs (ANA)

A

SLE

68
Q

Associated with Anti-smith Abs

A

SLE

69
Q

Associated with Anti-dsDNA Abs

A

Lupus nephritis

70
Q

Associated with Anti-Jo-1 Abs

A

Polymyositis/Dermatomyositis

71
Q

Associated with Anti-SSA (anti-Ro)

A

Sjogren syndrome

72
Q

Associated with Anti-SSB (anti-La)

A

Sjogren syndrome

73
Q

Associated with Anti-U1-RNP Abs

A

Mixed CT disease

74
Q

Associated with Anti-desmoglein Abs

A

Pemphigus vulgaris

75
Q

Associated with Anti-acetylcholine receptor Abs

A

Myasthenia gravis

76
Q

Associated with Anti-endomysial (anti-tissue transglutaminase)

A

Celiac disease

77
Q

Associated with Anti-gliadin Abs

A

Celiac disease

78
Q

Associated with anti-mitochondrial Abs

A

Primary Biliary Cirrhosis

79
Q

Associated with Anti-smooth muscle Abs

A

Autoimmune Hepatitis

80
Q

Associated with anti-glutamate decarboxylase Abs

A

Type 1 Diabetes

81
Q

Associated with Anti-thyrotropin receptor Abs

A

Graves disease

82
Q

Associated with Anti-thyroid peroxidase (anti-TPO)

A

Hashimoto thyroiditis

83
Q

Anti-thyroglobulin

A

Hashimoto thyroiditis, Graves disease

84
Q

Anti-Basement membrane Abs

A

Goodpasture syndrome

85
Q

c-ANCA

A

Granulomatosis with polyangiitis (Wegener’s)

86
Q

p-ANCA

A

Pauci-immune crescentic glomerulonephritis
Churg-Strauss syndrome
Microscopic polyangiitis

87
Q

Which vaccines are dangerous for patients with egg allergy?

A

Influenza

Yellow fever

88
Q

What mediates Type I Hypersensitivity?

A

Free antigen cross-linkes IgE on presensitized mast cells and basophils –> triggers immediate release of vasoactive amines that act on post capillary venules (histamine and bradykinin)

89
Q

What mediates Type II Hypersensitivity?

A

Cytotoxic (Ab mediated); IgM an IgG bind to FIXED antigen on “enemy” cell and cause cellular destruction by opsonization/phagocytosis, complement mediated inflammation or Ab-mediated cellular dysfunction

90
Q

What is Serum sickness?

A

Type III hypersensitivity reaction where antibodies to foreign proteins are produced –> immune complexes form and are deposited in membranes where they fix complement (cause tissue damage); mostly caused by drugs; happens 5-10 days after antigen exposure

91
Q

What are signs of serum sickness?

A

Fever, urticaria, arthralgia, proteinuria, lymphadenopathy

92
Q

What is Arthus reaction?

A

Local subacute antibody mediated type III hypersensitivity reaction caused by intradermal injection of antigen; takes 4-12 hours

93
Q

What are signs of Arthus reaction?

A

Edema, necrosis, activation of complement

94
Q

Acute hemolytic transfusion reaction

A

Type II

95
Q

Acute rheumatic fever

A

Type II

96
Q

Arthus reaction

A

Type III

97
Q

Asthma

A

Type I

98
Q

Bee sting allergy

A

Type I

99
Q

Contact dermatitis

A

Type IV

100
Q

Eczema

A

Type I

101
Q

Graves disease

A

Type II

102
Q

Guillain Barre syndrome

A

Type IV

103
Q

GVHD

A

Type IV

104
Q

Hashimoto thyroiditis

A

Type IV

105
Q

ITP

A

Type II

106
Q

MS

A

Type IV

107
Q

Myasthenia gravis

A

Type II

108
Q

PAN

A

Type III

109
Q

Peanut allergy

A

Type I

110
Q

Poststreptococcal GN

A

Type III

111
Q

RA

A

Type III

112
Q

Seasonal allergic rhinitis

A

Type I

113
Q

SLE

A

Type III

114
Q

What is the starting point for the Classic complement pathway?

A

IgG or IgM recognize C1

115
Q

What is C3b important for?

A

Opsonization

116
Q

What are the two most important opsonins?

A

C3b and IgG

117
Q

What are C3a and C5a important for?

A

Anaphylaxis
C3a - stimulates mast cells and basophils
C5a - neutrophil chemotaxis

118
Q

a. What happens if you are deficient in C1 esterase inhibitor?
b. What drug is C/I?

A

a. Hereditary angioedema (from elevated Bradykinin)

b. ACE inhibitors are C/I

119
Q

What happens if you are deficient in C3?

A

Recurrent pyogenic sinus and respiratory infections (Strep pneumo and H influenzae)
Also increased susceptibility to type III hypersensitivity and pyelonephritis

120
Q

What happens if you are deficient in C5b-C9 proteins?

A

Susceptible to recurrent Neisseria bacteremia

121
Q

a. What is DAF?

b. What happens if you have DAF deficiency?

A

a. GPI anchored enzyme (CD55)

b. Causes complement mediated lysis of RBCs and Paroxysmal Nocturnal Hemoglobinuria

122
Q

What kinds of organisms are asplenic patients susceptible to?

A

Encapsulated bacteria

123
Q

Even Some Pretty Nasty Killers Have Shiny Bodies

A 
E. coli
Streptococcus pneumo
Pseudomonas aeruginosa
Neisseria meningitidis
Klebsiella pneumoniae
Haemophilus influenza
Salmonella typhi
Group B Streptococcus
124
Q

Why would patient be missing spleen?

A

Trauma
Sickle cell patient
Hereditary spherocytosis - RBCs are defective and spleen keeps removing them

125
Q

What are macrophages activated by? What cells produce it?

A

IFNy

Produced by TH1 and NK cells

126
Q

Which cytokines do macrophages make?

A

IL1
IL6
TNFa

127
Q

What does IL-12 do?

A

Induces differentiation of T cells into TH1 cells

Activates NK cells

128
Q

What are the neutrophil chemotactic factors?

A

IL8, C5a, leukotriene B4

129
Q

What is Aldesleukin? What is it used for?

A

Recombinant IL-2 used for renal cell carcinoma and metastatic melanoma

130
Q

What are Filgrastim and Sargramostim? What are they used for?

A

Recombinant GM-CSF used for recovery of bone marrow

131
Q

What is Oprelvekin?

A

Recombinant IL-11 used for thromobocytopenia

132
Q

What is recombinant IFN-a used for?

A

Hepatitis B/C, Kaposi sarcoma, malignant melanoma, genital warts, hairy cell leukemia

133
Q

What is recombinant IFN-b used for?

A

Multiple sclerosis

134
Q

What is recombinant IFN-y used for

A

Chronic Granulomatous Disease

135
Q

What cytokines do TH1 cells produce?

A

IL-2 and IFNy

136
Q

What cytokine inhibits macrophage activation?

A

IL-10

137
Q

What does IL-10 inhibit?

A

Production of TH1 cells and macrophage activation

138
Q

What inhibits production of TH2 cells?

A

IFNy

139
Q

What muscles and nerves are derived from third branchial arch?

A 
Stylopharyngeus muscle
Glossopharyngeal nerve (IX)
140
Q

What kind of drug is used in treatment of Myasthenia gravis?

A

Acetylcholinesterase inhibitors like Pyridostigmine, Physostigmine

141
Q

What cytokines enhance NK cell activity?

A

IL-12
IL-2
IFN-a
IFN-b

142
Q

What do patients with common variable immunodeficiency have increased risk of later in life?

A

Autoimmune disease and lymphoma

143
Q

Complications of Sjogren’s syndrome

A 
Dental caries (decreased saliva production)
mucosa associated lymphoid tissue lymphoma (UNILATERAL PAROTID ENLARGEMENT)

Step 1 AB (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions